Dement Neurocogn Disord.  2014 Dec;13(4):139-145. 10.12779/dnd.2014.13.4.139.

Cognitive Intervention in a Patient with Carbon Monoxide Intoxication

• Oh JH
• Kim GW
• Choi SH
• Jeong JH
• Na HR
• Kim JE
• Na DL
• Hong CH
• Kim EJ

• KMID: 2443079
• DOI: http://doi.org/10.12779/dnd.2014.13.4.139

Abstract

BACKGROUND
Cognitive intervention (CI) is a nonpharmacological approach used to compensate for cognitive impairment. It is categorized into cognitive training, cognitive stimulation and cognitive rehabilitation. Several studies showed that CI could induce cognitive enhancement and reduction of risk for future cognitive decline in patients with brain injury. We investigated effects of CI on cognitive functions and brain glucose metabolism based on serial cognitive assessments and [18F]-Fluorodexoxyglucose positron emission tomography (FDG-PET) in a patient with carbon monoxide (CO) intoxication.
METHODS
A 40-year-old man presented with memory impairment and abnormal behaviors such as apathy, indifference, and perseveration 2-month after CO intoxication. Brain magnetic resonance image (MRI) demonstrated high signal changes in the bilateral basal ganglia, hippocampus and the subcortical white matter on T2 weighted images. FDG-PET also showed glucose hypometabolism in the bilateral hippocampus, basal ganglia, and the subcortical white matter. A detailed neuropsychological evaluation revealed multiple cognitive impairments in memory, language and frontal functions. He received twice a week sessions of 60-minute group-based cognitive intervention for 12 weeks. Several neuropsychological examinations and FDG-PETs were conducted at baseline and after CI.
RESULTS
After CI, he showed improvements in memory and frontal functions compared with baseline performances. These cognitive improvements persisted by the 7-month follow-up. The extent of glucose hypometabolism was decreased 1-month after CI, however increased 8-month after CI.
CONCLUSIONS
This case study suggested that CI could enhance cognitive functions and improve glucose metabolism in a patient with CO intoxication. Also, the effects of CI on cognitive functions seem to be last at least 7-month after training.

Keyword

Neuroplasticity; Neuropsychology; Cognitive intervention; Carbon monoxide intoxication; FDG-PET

MeSH Terms

Adult
Apathy
Basal Ganglia
Brain
Brain Injuries
Carbon Monoxide*
Follow-Up Studies
Glucose
Hippocampus
Humans
Memory
Metabolism
Neuronal Plasticity
Neuropsychology
Positron-Emission Tomography
Rehabilitation
Carbon Monoxide
Glucose

Figure

• 

  Fig. 1 Fluid-attenuated inversion recovery axial images (A) 3 days after CO intoxication show high signal intensities in the bilateral globus pallidus, putamen, hippocampus, cerebellum, and subcortical white matter. [18F]-Fluorodeoxyglucose positron emission tomography (FDG-PET) axial images taken 5 months after onset (baseline) showed glucose hypometabolism in the bilateral hippocampus, basal ganglia, and the subcortical white matter. Hypometabolic regions were examined using statistical parametric mapping PET analysis before (C), and 1 month (D) and 8 months (E) after cognitive intervention (CI) which were compared with those of 3 age-matched healthy controls. The extent of hypometabolic regions was decreased in 1 month after CI, whereas that in 8 months after CI was increased compared to that before CI (uncorrected, p<0.001).

• 

  Fig. 2 Changes of performance in each cognitive domain: before and after CI. A percentage of raw score in each cognitive domain is plotted with 7 months follow-up.

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